Herpes viruses, particularly the ubiquitous herpes simplex viruses, have a complex pathogenesis, and have long been recognized to be responsible for a variety of syndromes in man. Our previous work was aimed at an initial definition of this pathogenesis. Most importantly, we showed that experimental latent infections could be established in the nervous system. We propose to continue and extend these pathogenetic studies in experimental systems. The principal models used will be Herpes simplex virus and Marek's disease virus in genetically defined strains of mice and chickens. Here, using immunologic, virologic, histologic, and biochemical methods, we will study the physiological basis for latency and reactivation.